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Biomedical subjects

I Krieger

Publications and source records attributed to I Krieger.

At least 19 recordsLinked to original sources
PubMed2001

Crystallization and preliminary characterization of crystals of the C-terminal half fragment of tropomodulin.

Tropomodulin (40 kDa) stabilizes the actin-tropomyosin filament by capping the P end (slow-growing end). The C-terminal half (C20, 20 kDa), an independently folded domain that is believed to be responsible for the P-end capping, has been crystallized. Crystals grew in the presence of Zn(2+) as the solution pH was increased from 3 towards the pI of the protein. The crystals belong to the trigonal space group R3. They have unit-cell parameters a = b = 69.6, c = 101.3 A (mean values, with a estimated standard deviation of 0.009 A) and diffract to 1.9 A resolution when the frozen crystals were measured at 120 K on a rotating-anode X-ray source at 120 K.

Carrier Proteins↗
PubMed2000

Group interpersonal psychotherapy for patients with major depression disorder - pilot study.

BACKGROUND: This study evaluated the effectiveness of group interpersonal psychotherapy (IPT-G) for patients suffering from moderate to severe major depressive disorder (MDD), and who responded to antidepressant drugs during the acute phase treatment. METHODS: Subjects were allocated into two groups: in the study group subjects entered IPT-G while in the comparison group subjects continued with standard treatment. All subjects were assessed five times during and 6 months after the termination of the IPT-G in a double-blind, matched-control design. RESULTS: Subjects who participated in the IPT-G demonstrated significant improvement of their depressive symptoms compared to those who received the standard treatment both during the group therapy and in a 6-month follow-up period. CONCLUSIONS: Our preliminary results suggest that IPT in a group setting might be effective for a subset of patients who respond to antidepressant medication. LIMITATIONS: Small group of patients, lack of different types of treatment as control groups.

Adult↗
PubMed2000

Domain structure of tropomodulin: distinct properties of the N-terminal and C-terminal halves.

The structure of tropomodulin, the unique capping protein for the pointed end (the slow-growing end) of an actin filament, was studied. An improved Escherichia coli expression system for chicken E-tropomodulin was established and tropomodulin was prepared, Tmod (N39), in which 15 amino acid residues from the original C-terminus are deleted at the DNA level. This expression and purification system accidentally co-produces an 11-kDa fragment with the original N-terminus (N11). By applying limited proteolysis to Tmod (N39), a 20-kDa C-terminal fragment (C20) was obtained. The limited proteolysis data, as well as the fluorescence spectrometry and CD analyses of Tmod (N39), C20 and N11, revealed that tropomodulin is an alpha-helical protein that consists of two distinct domains. The C-terminal half (20 kDa) is resistant to proteolysis, which suggests that this domain is tightly folded. In contrast, the N-terminal half is susceptible to proteolysis, indicating that in solution this half is likely to be extended or to form a highly flexible structure. Cross-linking experiments with glutaraldehyde indicated that Tmod (N39) and N11 can form complexes with tropomyosin, whereas C20 cannot. This confirms the previous report that the site(s) of interaction with tropomyosin resides in the N-terminal 11-kDa region of tropomodulin.

Amino Acid Sequence↗
PubMed1996

[Homosexuality].

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Homosexuality↗
PubMed1987

Tryptophan deficiency and picolinic acid: effect on zinc metabolism and clinical manifestations of pellagra.

In five experiments, rats were fed tryptophan (Tryp)-deficient diets with 6-12 micrograms/g zinc (Zn) and, in one experiment, a Zn-deficient diet to test the effect on clinical manifestations, plasma and bone Zn, and ability of picolinic acid (PA) or extra (12 micrograms/g) Zn to compensate. Tryp deficiency caused classical manifestations of pellagra although niacin intake was in excess of normal requirements. At marginal Zn intakes, oral PA caused a significant increase of plasma Zn and, compared with Tryp-adequate controls, Tryp deficiency resulted in lower plasma Zn and plasma:bone Zn ratios. Extra Zn (total 24 micrograms/g) was ineffective. Subcutaneous PA showed a tendency to lower plasma Zn. PA had no effect on clinical manifestations. We conclude that a Tryp metabolite other than nicotinic acid is necessary in the prevention of pellagra. Our hypothesis links this finding with the observed Tryp and PA effect on Zn metabolism.

Animals↗
PubMed1986

Transient neonatal zinc deficiency.

We report an infant who developed clinical manifestations of zinc deficiency during the first month of life although the diet was adequate for zinc and no other causes could be ascertained. The diagnosis was confirmed by low plasma-zinc concentrations and a positive response to zinc treatment. The fatty acid profile of plasma phospholipids was typical of zinc deficiency (ie, arachidonic acid was markedly decreased). The transient nature of this disorder was evident when no relapse occurred after cessation of zinc therapy and plasma-zinc and arachidonic acid concentrations remained normal. Several explanations for the development of transient neonatal zinc deficiency are offered. The observation demonstrates that occasional infants may have requirements for zinc that are beyond the intakes of the conventional RDA.

Blepharitis↗
PubMed1985

Gyrate atrophy of the choroid and retina. Early findings.

Examination of two sisters ages 2 years 10 months and 6 years four months with gyrate atrophy of the choroid and retina provided an opportunity for detailed clinical investigation. Although the chorioretinal lesions were confined to the peripheral retina in the older case and were quite minimal in the younger case, there was electroretinographic evidence of marked involvement of the cone and rod systems. These cases offer an opportunity to assess an arginine restricted diet in preventing the progress of the disease.

Atrophy↗
PubMed1984

Threonine dehydratase deficiency: a probable cause of non-ketotic hyperglycinaemia.

A patient with classical symptoms of non-ketotic hyperglycinaemia (NKH) is presented. Threonine dehydratase was undetectable in a liver autopsy specimen, which was obtained within 1 h of death and immediately frozen at -70 degrees C. Activities of four marker enzymes were normal. This represents the first documentation of an inborn error of threonine metabolism and a new explanation of NKH.

Glutamate Dehydrogenase↗
PubMed1984

Picolinic acid in acrodermatitis enteropathica: evidence for a disorder of tryptophan metabolism.

Three children with acrodermatitis enteropathica (AE) were treated with oral zinc dipicolinate (zinc-PA). The daily dose of zinc required to prevent exacerbations, when administered as the dipicolinate complex, was one-third the minimum amount of zinc required as the sulfate salt. The concentration of picolinic acid in the plasma of asymptomatic children with AE was significantly less than that of normal children. However, oral treatment with PA alone was ineffective. The plasma of the three AE children contained a measurable quantity of kynurenine which was undetectable in plasma from normal children. Absorption of an oral zinc load was normal. The results support the hypothesis that the genetic defect in AE is in the tryptophan pathway, although the role of PA in zinc metabolism remains to be defined.

Acrodermatitis↗
PubMed1983

Picolinic carboxylase activity in rat liver and kidney. I. Influence of growth, sex, gestation, lactation, and nutritional imbalance.

Picolinic acid (PA) is a metabolite of tryptophan that chelates trace metals, including zinc. Several recent observations have suggested a role for PA in zinc metabolism. The enzyme responsible for its formation is picolinic carboxylase (PC). We have measured PC in rats under a variety of conditions, using tissues that play a role in zinc metabolism. PC activity was demonstrated in liver and kidney and was not detectable in pancreas and brain. Activity was most pronounced in kidney. In male suckling rats, PC increased gradually, reaching maximum levels on the 21st day of life. Only liver PC showed marked variations under different physiological conditions. Liver PC was higher on the 21st day of life than in adulthood. It was higher in female than in male adult rats. In pregnant rats, liver PC decreased gradually toward the end of gestation, reaching the lowest point near delivery; however, a 12-fold increase occurred during lactation. Liver PC activity of rats with symptoms of pellagra showed a fivefold increase over controls with similar body weight, whereas liver PC of chronically starved rats showed only a twofold increase over controls with twice their body weight.

Age Factors↗
PubMed1982

Screening for metabolic disease in a metropolitan hospital.

Screening for metabolic diseases at Children's Hospital of Michigan, Detroit during 1978 and 1979 led to the discovery of 7.5 cases per year, representing a marked increase over previous years. Five cases of organic aciduria were identified during this two-year period by use of urinary gas chromatography. Four of these were found to have methylmalonic aciduria. The increase in detection rate was due to the addition of an organic acid screening technique and greater use of two standard screening tests. The yield of screening by these two tests also improved, which we attribute to the better use of specific criteria. Inclusion of a simple urine screening test for methylmalonic acid is recommended in the workup of infants with episodic vomiting, lethargy, acidosis, or catastrophic illness.

Amino Acid Metabolism, Inborn Errors↗
PubMed1982

Zinc dependency as a cause of chronic diarrhea in variant acrodermatitis enteropathica.

Two siblings with chronic diarrhea, growth failure, mood changes, and occasional cheilosis responded repeatedly to treatment with either pharmacologic doses of zinc or pancreatin (Viokase), and their symptoms were exacerbated after withdrawal of therapy. Pancreatic exocrine deficiency was ruled out in both cases. Proteolytic activity was 20% of normal in one infant tested. Plasma zinc concentration was normal. Plasma picolinic acid concentration was low in these two patients and in one previously reported patient (mean 3.6, normal 12.4 +/- 3.3 mumoles/liter). This is a characteristic shared with acrodermatitis enteropathica. The response to Viokase may be due to its content of picolinic acid and/or zinc or the correction of a deficiency of carboxypeptidase, a zinc-requiring enzyme.

Child, Preschool↗
PubMed1981

Inhibition of bone marrow stem cell growth in vitro by methylmalonic acid: a mechanism for pancytopenia in a patient with methylmalonic acidemia.

A 7-week-old infant with methylmalonic acidemia had pancytopenia and hypoplastic bone marrow. The patient responded to large doses of vitamin B12 treatment, and within 3 wk, the blood counts and bone marrow cellularity returned to normal. To understand the mechanism of marrow depression in this infant, we examined the effect of the patient's plasma and methylmalonic acid itself on the in vitro growth of bone marrow-committed stem cells. The patient's plasma obtained before B12 treatment completely inhibited the marrow cell growth, whereas the posttreatment plasma showed no inhibition. Methylmalonic acid when added to the culture dishes in concentrations comparable to those reported in plasma of methylmalonic acidemia patients, inhibited growth of marrow stem cells in a concentration-dependent fashion. On the other hand, 16 to 18 hr incubation of cells in the same concentration of methylmalonic acid did not affect the recovery of viability of the cells. The observations suggest that methylmalonic acid is inhibitory to the proliferation of marrow stem cells. The mechanism of inhibition is yet to be elucidated.

Bone Marrow↗
PubMed1981

Genetic screening for mental retardation in Michigan.

The Michigan Department of Mental Health established a genetic screening laboratory in 1977 to provide diagnostic information on retarded patients. Of 727 patients screened during a 2-year period, a genetic diagnosis was established for 121 moderately to severely retarded patients. Genetic counseling was provided for 40 percent of their parents. A wide variety of chromosomal abnormalities, inborn errors of metabolism, and dysmorphic syndromes was discovered, including 16 instances of previously unknown familial conditions. This program has demonstrated a cost-effective method for determining genetic etiology in mental retardation and, in some instances, has led to prevention of mental retardation.

Abnormalities, Multiple↗